Homo sapiens
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PROVIDER: PRJNA248422 | ENA |
REPOSITORIES: ENA
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Project description:The paper describes a model of tumor invasion to bone marrow.
Created by COPASI 4.26 (Build 213)
This model is described in the article:
Modeling invasion of metastasizing cancer cells to bone marrow utilizing ecological principles
Kun-Wan Chen, Kenneth J Pienta
Theoretical Biology and Medical Modelling 2011, 8:36
Abstract:
Background: The invasion of a new species into an established ecosystem can be directly compared to the steps involved in cancer metastasis. Cancer must grow in a primary site, extravasate and survive in the circulation to then intravasate into target organ (invasive species survival in transport). Cancer cells often lay dormant at their metastatic site for a long period of time (lag period for invasive species) before proliferating (invasive spread). Proliferation in the new site has an impact on the target organ microenvironment (ecological impact) and eventually the human host (biosphere impact).
Results: Tilman has described mathematical equations for the competition between invasive species in a structured habitat. These equations were adapted to study the invasion of cancer cells into the bone marrow microenvironment as a structured habitat. A large proportion of solid tumor metastases are bone metastases, known to usurp hematopoietic stem cells (HSC) homing pathways to establish footholds in the bone marrow. This required accounting for the fact that this is the natural home of hematopoietic stem cells and that they already occupy this structured space. The adapted Tilman model of invasion dynamics is especially valuable for modeling the lag period or dormancy of cancer cells.
Conclusions: The Tilman equations for modeling the invasion of two species into a defined space have been modified to study the invasion of cancer cells into the bone marrow microenvironment. These modified equations allow a more flexible way to model the space competition between the two cell species. The ability to model initial density, metastatic seeding into the bone marrow and growth once the cells are present, and movement of cells out of the bone marrow niche and apoptosis of cells are all aspects of the adapted equations. These equations are currently being applied to clinical data sets for verification and further refinement of the models.
To cite BioModels Database, please use: BioModels Database: An enhanced, curated and annotated resource for published quantitative kinetic models .
To the extent possible under law, all copyright and related or neighbouring rights to this encoded model have been dedicated to the public domain worldwide.
Please refer to CC0 Public Domain Dedication for more information.
2024-09-02 | BIOMD0000000793 | BioModels
Project description:The paper describes a model of tumor invasion to bone marrow.
Created by COPASI 4.26 (Build 213)
This model is described in the article:
Modeling invasion of metastasizing cancer cells to bone marrow utilizing ecological principles
Kun-Wan Chen, Kenneth J Pienta
Theoretical Biology and Medical Modelling 2011, 8:36
Abstract:
Background: The invasion of a new species into an established ecosystem can be directly compared to the steps involved in cancer metastasis. Cancer must grow in a primary site, extravasate and survive in the circulation to then intravasate into target organ (invasive species survival in transport). Cancer cells often lay dormant at their metastatic site for a long period of time (lag period for invasive species) before proliferating (invasive spread). Proliferation in the new site has an impact on the target organ microenvironment (ecological impact) and eventually the human host (biosphere impact).
Results: Tilman has described mathematical equations for the competition between invasive species in a structured habitat. These equations were adapted to study the invasion of cancer cells into the bone marrow microenvironment as a structured habitat. A large proportion of solid tumor metastases are bone metastases, known to usurp hematopoietic stem cells (HSC) homing pathways to establish footholds in the bone marrow. This required accounting for the fact that this is the natural home of hematopoietic stem cells and that they already occupy this structured space. The adapted Tilman model of invasion dynamics is especially valuable for modeling the lag period or dormancy of cancer cells.
Conclusions: The Tilman equations for modeling the invasion of two species into a defined space have been modified to study the invasion of cancer cells into the bone marrow microenvironment. These modified equations allow a more flexible way to model the space competition between the two cell species. The ability to model initial density, metastatic seeding into the bone marrow and growth once the cells are present, and movement of cells out of the bone marrow niche and apoptosis of cells are all aspects of the adapted equations. These equations are currently being applied to clinical data sets for verification and further refinement of the models.
To cite BioModels Database, please use: BioModels Database: An enhanced, curated and annotated resource for published quantitative kinetic models .
To the extent possible under law, all copyright and related or neighbouring rights to this encoded model have been dedicated to the public domain worldwide.
Please refer to CC0 Public Domain Dedication for more information.
2024-09-02 | BIOMD0000000795 | BioModels
Project description:Identification of genes associated with bone metastatic breast cancer cells
| PRJNA221792 | ENA
Project description:Identification of CNA associated with bone metastatic breast cancer cells
| PRJNA221790 | ENA
Project description:Bone-marrow-derived mesenchymal stem cells promote breast cancer metastasis
| PRJNA102435 | ENA
Project description:Comparing gene-expression profiles between bone-metastatic vs. non bone-metastatic human prostate cancer cells
| PRJNA185441 | ENA
Project description:Breast tumor cells were found to remodel the bone marrow vascular microenviornment to support metastatic expansion. To identify tumor-derived factors that stimulate marrow endothelium, we studied the transcriptomes of four isogenic murine mammary tumor cell lines, 4T1.2, 4T1, 66cl4 and 67NR. To gain insight into the host vasculature in response to tumor colonization, we analysed the transcriptional signatures of EMCNhi/CD31hi endothelial cells extracted from heavily infiltrated bone marrow stroma (Metastatic) and from adjacent tumour-free bone marrow stroma (Non-metastatic), as well as from healthy bones (Control). This SuperSeries is composed of the SubSeries listed below.
2021-09-16 | GSE160102 | GEO
Project description:Metastases of breast cancer is a prevalent problem with over 25% of patients suffering with metastatic disease. Of the patients that present with metastatic disease, the majority are estrogen receptor positive (ER+) and have skeletal metastases. These skeletal metastases can cause several issues including pathological fractures, chronic pain, and hypercalcemia. Currently, there are not any cures for metastatic breast cancer in bone and only therapies to mediate the osteolysis caused by breast cancer. The bone microenvironment presents various physical forces that can act on the tumor cell that has been studied in ER- cells, however, the physical forces on ER+ tumor cells have not been widely evaluated. In this study, we explored the transcriptional changes that occur at different matrix rigidities associated with the bone microenvironment (bone marrow: 0.5 kPa to 32 kPa; cortical and trabecular bone – 2 x 107 kPa). We observed that lower stiffnesses contributed to increased gene signatures associated with interleukin signaling. Additionally, we observed that downstream estrogen signaling outputs were modified. These interesting findings give us insights on what may be changing when ER+ tumor cells encounter rigidities associated with the bone microenvironment.
2024-09-09 | GSE274519 | GEO
Project description:Bone is the most common metastasis site in patients with breast cancer, and approximately up to 80% of patients with advanced breast cancer (BC) develop bone metastasis (BM), which leads to a worse prognosis with a median survival of 16 months and skeletal-related events (SREs), including severe bone pain, pathological fracture, hypercalcemia and lethal complications. Using quantitative proteomics mass-spectrometry (MS) analysis of low bone-metastatic BC cells (MDA-MB-231) and high bone-metastatic BC cells (SCP2), we identified an unreported breast cancer (BC) cells–secreted microprotein, LINC00263-P, encoded by lincRNA LINC00263 and clinically associated with BC bone-tropism.
2025-01-06 | PXD059452 |
Project description:VEGF related gene expression signatures of breast cancer cells
| PRJNA362586 | ENA